Artificial Lung Created !

Researchers have created an artificial lung that uses air as a ventilating gas instead of pure oxygen - as is the case with current man-made lungs, which require heavy tanks of oxygen that limit their portability. The prototype device was built following the natural lung's design and tiny dimensions and the researchers say it has reached efficiencies akin to the genuine organ. With a volume roughly the same as a human lung, the device could be implanted into a person and even be driven by the heart.

The artificial lung is filled with breathable silicone rubber versions of the blood vessels that branch down to a diameter less than one-fourth of human hair. It was created by first building a mould with miniature features and then layering on a liquid silicone rubber that solidified into artificial capillaries and alveoli. They air and blood channels were then separated with a gas diffusion membrane.

By making the parts of the artificial lung on the same scale as the natural lung, the researchers say they were able to create a very large surface-area-to-volume ratio and shrink the distances for gas diffusion compared to the current state-of-the-art. In comparison to current artificial lung systems that require pure oxygen due to their inefficient oxygen exchange, tests of the new artificial lung using pig blood showed a three to five times improvement in oxygen exchange efficiency over current devices. It is this efficiency that enables the new artificial lung to use plain air instead of pure oxygen as the ventilating gas.

Blood is injected into the device's fluid inlet, while air is fed into the gas inlet. Oxygen molecules diffuse across the gas exchange membrane into the blood on the way to the blood outlet, while carbon dioxide in the blood fed into the device would diffuse across the membrane to be released through the air outlet.

"Based on current device performance, we estimate that a unit that could be used in humans would be about 6 inches by 6 inches by 4 inches tall, or about the volume of the human lung. In addition, the device could be driven by the heart and would not require a mechanical pump," said Joe Potkay, a research assistant professor in electrical engineering and computer science at Case Western Reserve University.

Potkay says the device is a major step towards an easily portable and implantable artificial lung and the team envisions patients using the technology while allowing their own diseased lungs to heal, or implanting one while awaiting a lung transplant.

Potkay's team, which includes Brian Cmolik, MD, an assistant clinical professor at Case Western Reserve School of Medicine, and Michael Magnetta and Abigail Vinson, biomedical engineers and third-year students at Case Western Reserve University School of Medicine, is now collaborating with researchers from Case Western Reserve's departments of biomedical engineering and chemical engineering to develop a coating to prevent clogging in the narrow artificial capillaries and on construction techniques needed to build a durable artificial lung large enough to test in rodent models of lung disease.

The Case Western Reserve University researchers expect to have human-scale artificial lungs in use in clinical trials within a decade.

Source: Gizmag

Trypophobia a Real Phobia? (Creepy Clustered Holes)

If you’re like me and you have a visceral reaction to the image above—if it makes your skin crawl, your hair hurt, and your stomach turn—you can count yourself among the trypophobic. According to its Facebook page, which is more than 4,000 members strong, trypophobia is fear of clustered holes. It is usually small holes in organic objects, such as lotus seed heads or bubbles in batter, that give trypophobics the extreme willies, triggering reactions like itchy skin, nausea and a general feeling of discomfort. 

Although this may be of no comfort to those who suffer from it, trypophobia is simply one of an infinite number of fears that people experience, some more idiosyncratic than others. The onlinePhobia List, run by an amateur etymologist, contains the names of hundreds of fears, from the well-known (fear of heights: acrophobia) to the fringe (fear of the great mole rat: zemmiphobia). Trypophobia hasn’t made the list yet.

According to Martin Anthony, a psychologist at Ryerson University in Toronto, past-president of the Canadian Psychological Association and author of The Anti-Anxiety Workbook, with the exception of a few terms (agoraphobia, claustrophobia and arachnophobia among them), professionals who study and treat phobias tend not to use all the Latin and Greek names that get tossed around on message boards and in the press.

Anthony wasn’t surprised to hear that some people have an intense aversion to clustered holes because “people can be afraid of absolutely anything.” The factors that contribute to fears and phobias include traumatic experiences (getting bitten by a dog leading to a fear of dogs, for example), observational learning (watching others be afraid of heights), information and instruction (learning to fear being alone in the dark after watching too many horror movies), and various biological factors (like an inherited predisposition to anxiety). “Although the studies on causes of fears have all focused on more common ones, such as spiders and snakes, there is no reason to think that different factors would be responsible for more unusual fears, Anthony says.

Trypophobia may also be catching. An element of so-called emotional contagion seems to be at work on Facebook, where some group members say they didn’t realize they were trypophobic until they started reading others’ comments and clicking on the pictures. “It’s not unusual to laugh harder at a funny movie if others around you are laughing,” Antony explains. “In the same way, we may be more likely to experience fear in a particular moment if others around us are fearful.” For me, however, all it took was a verbal mention of a “fear of small holes” to illicit a shudder. I became disgusted before looking at a single gnarly image of a skin graft or lamprey eel (look ’em up) or reading an online comment. I also immediately assumed that we were talking about biologic objects—holes in wood, in particular. Clearly, in me the fear was preexisting.

One trypophobic reported on Facebook that her fear stems back to childhood, when she had a Renaissance Faire dagger with a handle covered in little holes. Another member wrote: “I was stung by a bee in high school on my outer thigh. I had an allergic reaction, and my skin started to swell. The swelling was so bad, I could see each individual pore on my leg and I freaked out. Since then, I have not been able to look at clusters of holes without getting the heebie-jeebies.” Just. Gross.

Fear and disgust often go hand in hand, Anthony says. “Evolutionarily speaking, almost all of the things that arouse a strong disgust-reaction--spiders, mice, blood, vomit--are things that could have been triggers for fear of illness.” Perhaps the same could be true for little holes, especially in natural objects where they seem particularly out of place. I suspect that we’re disgusted by pockmarked objects because they don’t look quite “right”; these perceived deformities signal danger, which we manifest as revulsion. But then again, a fear of asymmetry (another form of things looking not quite right) in some people with obsessive-compulsive disorder is not associated with disgust, Antony says. Perhaps holes, particularly in organic objects, subconsciously remind us of the symptoms of contagious illnesses that affect the skin, such as the rash or blisters associated with measles and chicken pox, respectively. All of this, of course, is speculation, and just goes to show how little we know about trypophobia.

Masai Andrews hopes that will change. Andrews, who runs Trypophobia.com, founded the Facebook group page in 2009 when he was a sociology minor at SUNY-Albany. “I started the website and Facebook page because I suspected this was a very common phobia and I wanted a place where people could compile information,” Andrews says. “It is my hope that one day the academic and scientific communities will, at the very least, acknowledge the aversion to holes and certain patterns.”

When that happens, a Wikipedia page dedicated to the fear should follow. Surprisingly, one doesn’t exist today. “I can barely keep a page up on the subject without it getting taken down,” Andrews says. In March 2009 the powers that be at Wikipedia determined trypophobia to be a “likely hoax and borderline patent nonsense.” The deletion page also says that Wikipedia is “not for things made up one day.” As for who actually made the word up, that distinction probably belongs to a blogger in Ireland named Louise, Andrews says. According to an archived Geocities page, Louise settled on “trypophobia” (Greek for “boring holes” + “fear”) after corresponding with a representative at the Oxford English Dictionary. Louise, Andrews and trypophobia Facebook group members have petitioned the dictionary to include the word. The term will need to be used for years and have multiple petitions and scholarly references before the dictionary accepts it, Andrews says. I, for one, would prefer to forget about it forever.

Want to find out if you’re trypophobic? Take this quick visual test. But beware: You may be skipping lunch today.

Source: Popsci

Newly Found Gonorrhea Superbug Resists All Existing Antibiotics

A new strain of the gonorrhea bacteria can resist all available antibiotics, doctors say. Gonorrhea is one of the world’s most common sexually transmitted diseases, so this could portend a major threat to public health.

This should actually not be surprising, because for some time now, just one class of drug has been able to successfully treat the infection.

Now researchers in Sweden and Japan identified a new variant of Neisseria gonorrhoeae, the bug that causes gonorrhea, that can survive that last remaining drug, the cephalosporin-class antibiotics. Researchers isolated the strain from the throat of a sex worker in Japan, the Los Angeles Times reports.

“This is both an alarming and a predictable discovery,” said Dr. Magnus Unemo, of the Swedish Reference Laboratory for Pathogenic Neisseria, in a statement. The bacteria has been evolving to resist antibiotics since they became the standard treatment for the infection in the 1940s, during World War II.

The researchers were able to pinpoint four new genetic mutations that enable the bacteria’s resistance. Even worse, it readily passes on this resistance to other strains, increasing their resistance 500-fold, the Times says.

Gonorrhea is a particularly troubling and interesting bug. It is one of the only diseases that is unique to our species, and it’s one of the oldest known human pathogens. Earlier this year, researchers found a fragment of human DNA in the genome of Neisseria gonorrhoeae, evidence that it has adapted to its hosts quite well. The bacterium apparently picks up a genetic sequence from the host it’s infecting, according to that research, which was published in February. This may lend N. gonorrhoeae the ability to develop different strains of itself — and can explain why it has been so effective at morphing to evade antibiotics’ assaults.

The first treatments against gonorrhea used sulfonamides, but the bacteria evolved to resist it; later treatments used penicillin, which also no longer works; tetracyclines and fluoroquinolines like Cipro don’t either, the L.A. Times notes.

It’s too early to tell whether this new super-STD is already spreading, but it’s likely to do so unless new therapies are developed, Unemo said.

Gonorrhea impacts about 700,000 Americans every year, according to the Centers for Disease Control and Prevention. If untreated, it can lead to serious health complications in both genders, the CDC says. It can lead to infertility in women and especially men, and it increases the risk of transmitting other STDs, like HIV. Babies born to infected mothers are at high risk of developing serious infections and blindness. About 3 to 4 percent of the time, it can spread to the skin, blood, heart and joints in infected adults.

The report on this new strain was presented Sunday at a Quebec City meeting of the International Society for Sexually Transmitted Disease Research. Just last Thursday, the CDC reported growing numbers of gonorrhea infections that require unusually high doses of cephalosporins to cure them, the LA Times said. For now, treatment should include cephalosporins and the antibiotic azithromycin, while the CDC and National Institutes of Health work on new drugs.

Source: Popsci via Eurekalert

Spanish Surgeons Conduct the World's First Double Leg Transplant

This month in amazing medical procedures, it’s all about Europe. Last week we learned that a pan-European team of researchers and doctors have successfully pulled off the first transplant of a synthetic organ grown from the patient’s own stem cells. This week, the world’s first double leg transplant was successfully executed in Spain.

The male patient has not yet been identified, but the 13-hour surgery that involved painstakingly reattaching each of his nerves and blood vessels to those in his new legs has been deemed a success. The patient is awake and reportedly quite pleased with his new biological hardware, though it will take a good deal of immunotherapy to ensure his body doesn’t reject the new limbs, and another several months before he can be expected to gain any feeling in the transplanted extremities.

Leg amputees usually aren’t good candidates for limb transplants because there are very good prostheses available and the procedure is quite difficult. In this case, the patient had lost his legs in an accident, and the amputation had occurred so high on the thigh as to rule out attaching prosthetic limbs. With no alternative, doctors green lit the procedure. They hope to have the patient moving his knees in a few weeks, and perhaps have him walking in physical therapy within six months.

Source: Popsci via New Scientist

Discovery of natural antibody offers hope for a near-universal flu vaccine

Every year in the lead up to flu season, those at high risk of infection, such as the young, the elderly and those who are immune-compromised, head off to the doctor for a jab in the hopes it will protect them from the flu. However, influenza vaccines have a number of shortcomings that means even those who have been vaccinated may still get influenza. Researchers at the Scripps Research Institute and Dutch biopharmaceutical company Crucell have now found a broadly acting antibody that could lead to a single, near-universal flu vaccine to replace annually changing vaccines.

The high mutation rate of the influenza virus means that any particular influenza vaccine will usually grant protection for a few years at most. So every year, the World Health Organization predicts which strains of the virus are most likely to be circulating in the next year, allowing pharmaceutical companies to develop vaccines that will provide the best immunity against these strains. But with the large number of strains and the fact it takes pharmaceutical manufacturers six months to formulate and produce the millions of doses required, a new or overlooked strain can become prominent in the interim, meaning that even those who have been vaccinated may become infected.

Overcoming basic flu-virus defense mechanism

Attempts to create a vaccine that works against a wide set of strains and therefore provides protection against unforeseen strains have encountered difficulties relating to the structures that hold the virus itself. These spherical or filamentous envelopes are studded with mushroom-shaped hemagglutinin (HA) proteins, whose more accessible outer structures effectively serve as decoys for a normal antibody response.

"The outer loops on the HA head seem to draw most of the antibodies, but in a given strain these loops can mutate to evade an antibody response within months," said Ian Wilson, who is the Hansen Professor of Structural Biology and a member of the Skaggs Institute for Chemical Biology at Scripps Research.

This means that antiviral drugs aimed at these and other viral targets will also lose effectiveness as flu populations evolve. The researchers therefore sought to find and attack structures on flu viruses that are relatively unvarying and functionally important.

After sifting through the blood of people who had been immunized with flu vaccines, Crucell's Jaap Goudsmit discovered an antibody called CR6261 that bound to one such vulnerable structure. In mice, Goudsmit's team found that an injection of CR6261 could prevent or cure an otherwise-lethal infection by about half of flu viruses. These included H1 viruses such as H1N1, strains of which were responsible for the 1918 Spanish Flu and 2009 Swine Flu global pandemics.

The Crucell researchers approached Wilson, whose team determined the three-dimensional molecular structure of CR6261 and its binding site on HA, which was reported in Science in 2009. That binding site, or "epitope," turned out to be on HA's lower, less-accessible stalk portion and the binding of CR6261 to that region apparently interferes with flu viruses' ability to deliver their genetic material into host cells and start a new infection.

Not good enough

Not content with that, the Crucell researchers subsequently set about looking for an antibody that could neutralize all of the remaining flu viruses unaffected by CR6261. They recently found success with one called CR8020, which they say powerfully neutralizes a range of human-affecting flu viruses, including H3 and H7 subtypes, in lab-dish tests and in mice.

Utilizing the same technique used with CR6261, the researchers were able to determine the antibody's structure and its precise epitope on the viral HA protein.

"It's even lower on the HA stalk than the CR6261 epitope; in fact it's closer to the viral envelope than any other influenza antibody epitope we've ever seen," said Damian Ekiert, a graduate student in the Scripps Research Kellogg School of Science and Technology who is working in the Wilson laboratory.

Crucell is about to begin tests of the CR6261 antibody in human volunteers and expects to eventually begin similar trials of CR8020. If those trials succeed, aside from a vaccine the two antibodies could be combined and used in a "passive immunotherapy" approach.

"This would mainly be useful as a fast-acting therapy against epidemic or pandemic influenza viruses," said Wilson. "The ultimate goal is an active vaccine that elicits a robust, long-term antibody response against those vulnerable epitopes; but developing that is going to be a challenging task."

The Scripps Research and Crucell team's paper, "A Highly Conserved Neutralizing Epitope on Group 2 Influenza A Viruses," is published in the journal Science Express.

Source: Gizmag

A Biocomputer Can Now Detect Multiple Signs of Disease from Inside the Body

Wouldn’t it be easier to deal with disease if our bodies just fixed themselves? That’s asking quite a bit from our physiologies, but Israeli researchers are working on tiny nano-computers that could do the job for us. They envision tiny machines made of biomolecules that autonomously troll the body looking for disease, computing a diagnosis and delivering drugs all at the same time. It’s a long way off, but they’re making progress--they’ve just developed a biomolecular computer that can autonomously identify multiple molecules at the same time.

From a biomolecular computing standpoint (as well as from a diagnostics standpoint), that’s pretty huge. The researchers have previously demonstrated a biomolecular computer that could sense disease indicators one at a time. Existing in a two state system, it essentially was programmed in a “yes” state for a certain disease indicator. It then performed a series of computation steps, checking for one mRNA disease indicator after another.

If all the indicators of a certain disease are present, the biocomputer would end unchanged in the same “yes” state. If any of the indicators were not present, it would end in a “no” state. It was rudimentary, but it was a diagnosis if an imperfect one.

The breakthrough here is that the team’s biocomputer now can now detect disease indicators from a variety of sources--mRNA, miRNA, proteins, and a variety of small molecules like ATP. The new biocomputer also needs fewer interactions with disease indicators and is designed with fewer moving parts.

The idea is to someday create swarms of biomolecular nano-computers that can autonomously and continuously patrol our bodies for the signs of disease. Because they can now detect indicators from more than one source, diagnoses would be more accurate. And with more and better computation, the biomachines could also deliver the first round of preventative drugs to the site of burgeoning disease, acting as a first line of defense against infection.

Of course, all this is years--decades, really--away. The idea that of nanomachines--even ones constructed of biomolecules--swimming our bloodstreams loaded up with drug payloads is a bit anxiety-inducing. What if they malfunction or misdiagnose? What if they were to accidentally release too much of a drug at the wrong place at the wrong time, or to inadvertently mix the wrong drugs into a harmful pharmaceutical cocktail?

You might lose sleep at night wondering what the tiny machines inside of you were up to. Even so, the idea of constant, vigilant, autonomous oversight of every organ in the body is pretty tantalizing.

Source: Popsci via PhsyOrg

Lab Builds a Fully Functioning Artificial Small Intestine

California researchers have created a tissue-engineered small-scale small intestine in mice, a breakthrough for regenerative medicine and a step toward growing new intestines for humans. The process re-creates all the layers of cells that make up a functioning intestine.

Tissue engineering, which promises to rebuild or replace injured or failing body parts, has seen some major advancements in recent months, with biological scaffolds used to create new bones in rabbits and regrown muscle in humans. But it’s more difficult to make a complete organ, which has several types of cells that must all function properly.

The small intestine is a good subject for this type of study because it’s a particularly regenerative organ, said Dr. Tracy C. Grikscheit, the lead author of a paper on this research.

Grikscheit and colleagues at The Saban Research Institute of Children's Hospital Los Angeles took samples of mice intestinal tissue, including all the layers of cells — muscle cells and epithelial cells. Then the team transplanted the cells onto a polymer scaffold within the abdomen, a news release explains. Growth factor proteins encouraged the cells to replicate.

New small intestines grew on the scaffold, the researchers say, and they had all the constituents of a normal intestine. The new intestines “contained the most essential components of the originals,” according to the news release.

The research could someday be used to treat various intestinal disorders, including a particular gastrointestinal disease that affects premature babies, according to Children’s Hospital. An engineered replacement organ would conceivably last much longer than a transplant, if one is even available.

A paper on the research is published in the journal Tissue Engineering Part A.

Source: Popsci via Science Daily

Gastric bacterium protects against asthma and proves hygiene hypothesis

Electron micrograph of H. pylori

It's widely recognized that asthma rates have increased significantly since the 1960's and continue to rise. With increases in asthma and other allergic diseases centered on industrialized nations, a recent hypothesis suggested that the disappearance of specific microorganisms that populate the human body due to modern hygiene practices might be to blame. Now researchers claim they have confirmed this hypothesis by proving that a certain gastric bacterium provides reliable protection against allergy-induced asthma.

The hygiene hypothesis states that modern hygiene practices and overuse of antibiotics have led to a lack of early childhood exposure to infectious agents, symbiotic microorganisms and parasites, which has suppressed the natural development of the body's immune system. Scientists from the University of Zurichand the University Medical Center of the Johannes Gutenberg University Mainz are now saying that the increase in asthma could be put down to the specific disappearance of the gastric bacterium Helicobacter pylori (H. pylori) from Western societies.

H. pylori is a bacterium that is resistant to gastric acid and it is estimated that it could currently infect around half of the world's population. While it can cause gastritis, gastric and duodenal ulcers, and stomach cancer under certain conditions, over 80 percent of individuals infected with the bacterium are asymptomatic. However, even if the patient doesn't show any symptoms, H. pylori is often killed off with antibiotics as a precaution.

For their study, the researchers infected mice with H. pylori bacteria at different stages of their development. They found that mice that were infected at just a few days old developed immunological tolerance to the bacterium and reacted insignificantly or not at all to strong, asthma-inducing allergens. Mice that were not infected until they had reached adulthood, however, had a much weaker defense.

"Early infection impairs the maturation of the dendritic cells and triggers the accumulation of regulatory T-cells that are crucial for the suppression of asthma," explains Anne Müller, a professor of molecular cancer research at the University of Zurich.

The researchers also found that if the regulatory T-cells were transferred from infected mice to uninfected mice, they too enjoyed effective protection against allergy-induced asthma. Additionally, mice that had been infected early lost their resistance to asthma-inducing allergens if H. pylori was killed off in them using antibiotics.

According to lung and allergy specialist Christian Taube, a senior physician at III. Medical Clinic of the Johannes Gutenberg University Mainz, the new results that are published in the Journal of Clinical Investigation confirm the hypothesis that the increase in allergic asthma in industrial nations is linked to the widespread use of antibiotics and the subsequent disappearance of micro-organisms that permanently populate the human body.

"The study of these fundamental mechanisms is extremely important for us to understand asthma and be able to develop preventative and therapeutic strategies later on," he said.

Source: Gizmag

'Sensing skin' could detect cracks in concrete structures

Concrete may be one of the toughest buildings materials in common use but it does develop cracks over time, and in the case of structures such as buildings or bridges, it is imperative that those cracks are noticed before they lead to a collapse. While visual inspections are useful, they are also time-consuming, and may miss tiny but structurally-significant cracks. Some technologies have been developed to automate the process, such as rust sensors for steel-reinforced concrete. Now, an international team of scientists is proposing a system of flexible crack-detecting skins, that could be applied to the surfaces of concrete surfaces.

The "sensing skin" was developed by civil engineers at the Massachusetts Institute of Technology (MIT), working with physicists at Germany's University of Potsdam.

Structures such as bridges would simply have pieces of the skin glued onto any areas where cracks were considered likely to occur. The skin would contain patterns of capacitive rectangular patches, arranged in different patterns within the skin, depending on the type of stress that was likely - patches oriented diagonally to one another would work best for detecting cracks caused by shear, whereas horizontally-joined patches would be better for detecting sag in horizontal beams, for instance.

The capacitance of each patch (the amount of energy it was storing) would be altered by any movement underneath it, as would be caused by the formation of cracks. Once a day, a computer that was attached to the skin would send an electrical current through it, measuring the capacitance of each patch. If sharp differences were noted between adjacent patches, the computer would note the exact location, and then notify a human inspector of the discrepancy. This ability to pinpoint the location reportedly sets the system apart from other stress-detecting technologies, that don't provide such specific coordinates.

So far, the largest piece of the skin tested in laboratory conditions has measured 8 by 4 inches (20 by 10 cm). While a stretchy silicon fabric with silver electrodes was used initially, it proved to be too thin and flexible for some applications. It has since been replaced with a thermoplastic elastomer mixed with titanium dioxide, with the capacitive patches made from painted-on black carbon.

Source: Gizmag

Human Belly Button Is Home to Hundreds of Never-Before-Seen Species

Call it a twist on the study of gut bacteria. Scientists sampling DNA strains from the navels of volunteer donors have found 662 microbes that are apparently new to science, showing that the human navel is apparently a ripe environment for bacteria.

The Belly Button Biodiversity Project, run by scientists at North Carolina State University in Raleigh, has been analyzing navel swabs from a host of volunteers, as New Scientist explains. So far, they’ve found 1,400 distinct bacterial strains, nearly half of which have never been seen before.

The project was meant to interest people in microbiology and assuage the public’s concerns about microbes causing disease, but it’s also yielded plenty of new data about the human “microbiome,” the array of microorganisms that live inside (and on) us. The skin is still not that well studied, and researchers led by Rob Dunn and Jiri Hulcr at NC State wanted to examine belly buttons because, well, they’re harder to scrub than the rest of your body.

Science writers Carl Zimmer (who blogs at Discover) and Peter Aldhous (from New Scientist) each donated a swab, and while Aldhous’ sample failed to yield bacterial colonies, Zimmer’s sample was apparently flush with life. Some species in his microbiome have previously only been found in the ocean, he writes. Another one, a species called Georgenia, has only been found living in the soil in Japan. Zimmer has never been, he writes.

“It has apparently been to you,” Dunn told him.

The researchers have recorded a large number of new microbes, but most of them are found in small numbers, New Scientist reports. About 40 species account for around 80 percent of the bacterial populations of our belly buttons, Aldhous writes.

Something nice to think about when you're sunbathing over the holiday weekend — your swimsuit has plenty of company.

Source: Popsci via New Scientist

Spiders Fleeing Pakistan's Floodwater Take to the Trees

Last summer’s floods in Pakistan displaced millions of people--and millions of spiders. Although spiders rarely migrate to trees during natural disasters, the flooding was so heavy and prolonged, they had to climb trees and remain there. According to University of Akron biologist Todd Blackledge, who studies web-weaving spiders, some spin new webs each day. After weeks, the dense layers of silk, seen here in Sindh province, covered the trees--a result of continuous web spinning by the eight-legged refugees.

During a humanitarian-aid trip last December, Russell Watkins, a photographer with the British government agency the Department for International Development, encountered the web-veiled landscape. “I wasn’t prepared for the scale,” he says. “Literally thousands of trees and bushes over dozens of miles were shrouded. It really was very spooky.”

While the floods displaced spiders, the mosquitoes were surprisingly unaffected. The stagnant water should have provided prime breeding grounds for the insects, but local inhabitants noticed that there were far fewer mosquitoes than expected. Although the spiders could have accounted for some of the mosquito population drop, John Gimnig, an entomologist with the Centers for Disease Control and Prevention, says that shifts in climate affect mosquitoes more than spiders do.

Source: Gizmag

Preventing Heart Attack Using Magnetic fields

Overly-viscous blood can damage blood vessels and lead to heart attacks. Therefore, people who are at risk of heart attacks take medications such as Aspirin, in order to thin their blood. Such drugs can have unpleasant side effects, however, and can only be taken a certain number of times per day. Prof. Rongjia Tao, a physicist from Philadelphia's Temple University, now thinks he might have come up with a better way of thinning human blood - he subjects it to magnetic fields.

Tao had previously researched the use of magnetism for decreasing the viscosity of oil in engines and pipelines. Because blood contains iron, it turns out that it, too, becomes more fluid when magnetized.

In lab tests, Tao and Temple collaborator Ke "Colin" Huang subjected human blood samples to a magnetic field of 1.3 Telsa (roughly equivalent to an MRI) for approximately one minute. This polarized the red blood cells, which caused them to link together into short chains. These chains, because they are larger than single cells, tend to flow down the middle of blood vessels, instead of creating friction by moving against the inner walls. All told, he was able to decrease the viscosity of the samples by 20 to 30 percent.

The blood did return to its original viscosity once the magnetic field was removed, although it took several hours to do so. It is apparently safe to repeat the treatment over and over, however, as the function of the red blood cells does not appear to be affected.

"By selecting a suitable magnetic field strength and pulse duration, we will be able to control the size of the aggregated red-cell chains, hence to control the blood's viscosity," said Tao. "This method of magneto-rheology provides an effective way to control the blood viscosity within a selected range."

More work is required, although Tao hopes to ultimately make the treatment available as a preventative therapy.

The research is being published in the journal Physical Review E.

Source: Gizmag